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Research Article Free access | 10.1172/JCI107092
Department of Medicine, Duke University Medical Center, Durham 27710
Department of Surgery, Duke University Medical Center, Durham 27710
Veterans Administration Hospital, Durham, North Carolina 27705
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Department of Medicine, Duke University Medical Center, Durham 27710
Department of Surgery, Duke University Medical Center, Durham 27710
Veterans Administration Hospital, Durham, North Carolina 27705
Find articles by Rembert, J. in: JCI | PubMed | Google Scholar
Department of Medicine, Duke University Medical Center, Durham 27710
Department of Surgery, Duke University Medical Center, Durham 27710
Veterans Administration Hospital, Durham, North Carolina 27705
Find articles by Young, W. in: JCI | PubMed | Google Scholar
Department of Medicine, Duke University Medical Center, Durham 27710
Department of Surgery, Duke University Medical Center, Durham 27710
Veterans Administration Hospital, Durham, North Carolina 27705
Find articles by Oldham, H. in: JCI | PubMed | Google Scholar
Department of Medicine, Duke University Medical Center, Durham 27710
Department of Surgery, Duke University Medical Center, Durham 27710
Veterans Administration Hospital, Durham, North Carolina 27705
Find articles by Alexander, J. in: JCI | PubMed | Google Scholar
Department of Medicine, Duke University Medical Center, Durham 27710
Department of Surgery, Duke University Medical Center, Durham 27710
Veterans Administration Hospital, Durham, North Carolina 27705
Find articles by Sabiston, D. in: JCI | PubMed | Google Scholar
Published October 1, 1972 - More info
Pressure-flow measurements were obtained from the vein graft of 57 patients undergoing a single aorta-to-coronary bypass procedure.
The flow contour was similar to phasic left coronary artery flow in dogs except for a transient increase during systole possibly related to elongation of the graft. Flow was highest during bypass and decreased to a stable value 30 min after bypass. In 42 patients, flow at this time was 35±2 cm3/min (mean±sem).
No correlations were demonstrated between flow and the following: left vs. right grafts, presence or absence of collaterals, total vs. partial block, or the presence or absence of ventricular dyskinesis. In 32 patients, no correlation between these anatomic findings and the presence of reactive hyperemia was demonstrated. In 17 patients, occlusion of the graft for 10 sec resulted in a mean 51.5% flow debt repayment.
In nine patients, injection of 0.3 μg of isoproterenol into the graft increased flow from 45±6 to 69±9 cm3/min within 4-7 sec without changes in rate, pressure, time derivative of left ventricular pressure (LV dp/dt), or left ventricular end diastolic pressure (LVEDP). Maximum increases to 87±10 cm3/min occurred 12-20 sec after injection with concomitant changes in these parameters.
Intravenous infusion of norepinephrine did not change vascular resistance, whereas phenylephrine did. In six patients, injection of 0.2 μg of norepinephrine into the graft decreased flow from 49±6 to 25±5 cm3/min within 5-8 sec.
Intravenous infusion of 0.15 mg of nitroglycerin decreased coronary vascular resistance from 2.7±0.4 to 2.3±0.3 mm Hg/cm3 per min. In five patients, 0.12 mg of nitroglycerin injected into the graft increased flow from 46±7 to 71±13 cm3/min and lasted 20-40 sec.